The Biology of the PmrA PmrB Two-Component System: The Major Regulator of Lipopolysaccharide Modifications

The Biology of the PmrA PmrB Two-Component System: The Major Regulator of Lipopolysaccharide Modifications

The ability of gram-negative bacteria to resist killing by antimicrobial agents and to avoid detection by host immune systems often entails modification to the lipopolysaccharide (LPS) in their outer membrane. In this review, we examine the biology of the PmrA PmrB two-component system, the major re...

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Published in:Annual review of microbiology Vol. 67; no. 1; pp. 83 - 112
Main Authors: Chen, H. Deborah, Groisman, Eduardo A
Format: Journal Article
Language:English
Published: United States Annual Reviews 01-01-2013
Annual Reviews, Inc
Subjects:
Anti-Bacterial Agents - pharmacology
Antibacterial agents
antibiotic resistance
Antimicrobial agents
Bacteria
bacterial evolution
Bacterial Proteins - genetics
Bacterial Proteins - metabolism
Drug resistance
Ecology
feedback mechanisms
Gene expression
gene expression kinetics
Gene Expression Regulation, Bacterial
Gram-negative bacteria
horizontal gene transfer
Lipopolysaccharides - metabolism
Membranes
Pathogens
Salmonella typhimurium - drug effects
Salmonella typhimurium - genetics
Salmonella typhimurium - metabolism
Transcription Factors - genetics
Transcription Factors - metabolism
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Abstract The ability of gram-negative bacteria to resist killing by antimicrobial agents and to avoid detection by host immune systems often entails modification to the lipopolysaccharide (LPS) in their outer membrane. In this review, we examine the biology of the PmrA PmrB two-component system, the major regulator of LPS modifications in the enteric pathogen Salmonella enterica. We examine the signals that activate the sensor PmrB and the targets controlled by the transcriptional regulator PmrA. We discuss the PmrA PmrB-dependent chemical decorations of the LPS and their role in resistance to antibacterial agents. We analyze the feedback mechanisms that modulate the activity and thus output of the PmrA PmrB system, dictating when, where, and to what extent bacteria modify their LPS. Finally, we explore the qualitative and quantitative differences in gene expression outputs resulting from the distinct PmrA PmrB circuit architectures in closely related bacteria, which may account for their differential survival in various ecological niches.
AbstractList The ability of gram-negative bacteria to resist killing by antimicrobial agents and to avoid detection by host immune systems often entails modification to the lipopolysaccharide (LPS) in their outer membrane. In this review, we examine the biology of the PmrA/PmrB two-component system, the major regulator of LPS modifications in the enteric pathogen Salmonella enterica. We examine the signals that activate the sensor PmrB and the targets controlled by the transcriptional regulator PmrA. We discuss the PmrA/PmrB-dependent chemical decorations of the LPS and their role in resistance to antibacterial agents. We analyze the feedback mechanisms that modulate the activity and thus output of the PmrA/PmrB system, dictating when, where, and to what extent bacteria modify their LPS. Finally, we explore the qualitative and quantitative differences in gene expression outputs resulting from the distinct PmrA/PmrB circuit architectures in closely related bacteria, which may account for their differential survival in various ecological niches. [PUBLICATION ABSTRACT]
The ability of gram-negative bacteria to resist killing by antimicrobial agents and to avoid detection by host immune systems often entails modification to the lipopolysaccharide (LPS) in their outer membrane. In this review, we examine the biology of the PmrA/PmrB two-component system, the major regulator of LPS modifications in the enteric pathogen Salmonella enterica. We examine the signals that activate the sensor PmrB and the targets controlled by the transcriptional regulator PmrA. We discuss the PmrA/PmrB-dependent chemical decorations of the LPS and their role in resistance to antibacterial agents. We analyze the feedback mechanisms that modulate the activity and thus output of the PmrA/PmrB system, dictating when, where, and to what extent bacteria modify their LPS. Finally, we explore the qualitative and quantitative differences in gene expression outputs resulting from the distinct PmrA/PmrB circuit architectures in closely related bacteria, which may account for their differential survival in various ecological niches.
The ability of gram-negative bacteria to resist killing by antimicrobial agents and to avoid detection by host immune systems often entails modification to the lipopolysaccharide (LPS) in their outer membrane. In this review, we examine the biology of the PmrA PmrB two-component system, the major regulator of LPS modifications in the enteric pathogen Salmonella enterica. We examine the signals that activate the sensor PmrB and the targets controlled by the transcriptional regulator PmrA. We discuss the PmrA PmrB-dependent chemical decorations of the LPS and their role in resistance to antibacterial agents. We analyze the feedback mechanisms that modulate the activity and thus output of the PmrA PmrB system, dictating when, where, and to what extent bacteria modify their LPS. Finally, we explore the qualitative and quantitative differences in gene expression outputs resulting from the distinct PmrA PmrB circuit architectures in closely related bacteria, which may account for their differential survival in various ecological niches.
Author Groisman, Eduardo A
Chen, H. Deborah
AuthorAffiliation 1
Yale Microbial Diversity Institute, PO Box 27389, West Haven, Connecticut 06516
2
eduardo.groisman@yale.edu
3
Department of Microbial Pathogenesis
Howard Hughes Medical Institute, Boyer Center for Molecular Medicine, Yale University School of Medicine, New Haven, Connecticut 06536; email
AuthorAffiliation_xml – name: Howard Hughes Medical Institute, Boyer Center for Molecular Medicine, Yale University School of Medicine, New Haven, Connecticut 06536; email
– name: Yale Microbial Diversity Institute, PO Box 27389, West Haven, Connecticut 06516
– name:
– name: Department of Microbial Pathogenesis
– name: 3
– name: eduardo.groisman@yale.edu
– name: 2
– name: 1
Author_xml – sequence: 1
  givenname: H. Deborah
  surname: Chen
  fullname: Chen, H. Deborah
– sequence: 2
  givenname: Eduardo A
  surname: Groisman
  fullname: Groisman, Eduardo A
BackLink https://www.ncbi.nlm.nih.gov/pubmed/23799815$$D View this record in MEDLINE/PubMed
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Snippet The ability of gram-negative bacteria to resist killing by antimicrobial agents and to avoid detection by host immune systems often entails modification to the...
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SubjectTerms Anti-Bacterial Agents - pharmacology
Antibacterial agents
antibiotic resistance
Antimicrobial agents
Bacteria
bacterial evolution
Bacterial Proteins - genetics
Bacterial Proteins - metabolism
Drug resistance
Ecology
feedback mechanisms
Gene expression
gene expression kinetics
Gene Expression Regulation, Bacterial
Gram-negative bacteria
horizontal gene transfer
Lipopolysaccharides - metabolism
Membranes
Pathogens
Salmonella typhimurium - drug effects
Salmonella typhimurium - genetics
Salmonella typhimurium - metabolism
Transcription Factors - genetics
Transcription Factors - metabolism
Title The Biology of the PmrA PmrB Two-Component System: The Major Regulator of Lipopolysaccharide Modifications
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